Reliability of renal point-of-care ultrasound (POCUS) performed by pediatric postgraduates to diagnose hydronephrosis in infants

PurposePoint-of-care ultrasound (POCUS) has gained prominence in a variety of medical specialties due to advances in ultrasound technology. POCUS has not been fully integrated into pediatric residency training programs despite its widespread use and proven benefits. At our institution, renal POCUS is performed by pediatric residents for the evaluation of hydronephrosis, which is the main pathology for which ultrasound is used in the clinical practice of pediatric nephrology. This study was conducted to evaluate the quality of renal POCUS performed by pediatric residents in infants.MethodsFour pediatric residents, comprising two first-year and two second-year residents at Konyang University Hospital, participated in the study conducted from May 2021 to May 2022. All participants had completed our Point-of-Care Ultrasound (POCUS) training program. The study focused on infants admitted to the pediatric inpatient unit, identified by attending physicians as requiring renal ultrasound. All infants underwent their initial kidney ultrasound examination. Temporal alignment between renal Point-of-Care Ultrasound (POCUS) performed by pediatric residents and conventional ultrasound (USG) conducted by radiologists was asynchronous. Pediatric residents conducted POCUS sessions during scheduled radiologist appointments throughout the day, occurring either before or after the radiologist's examination. There was no mutual awareness of each other's results. Inter-observer agreement between radiologists and pediatric residents was compared for the presence or absence of hydronephrosis and its grade, which are primary considerations in pediatric renal ultrasound.ResultsOur study found that 53 infants (68.8%) were diagnosed with hydronephrosis using point-of-care ultrasound (POCUS), compared to 48 infants (62.3%) diagnosed with conventional ultrasound (USG). Among the POCUS examinations conducted by pediatric residents, hydronephrosis of SFU grades 1, 2, 3, and 4 were observed in 56.6%, 35.8%, 7.5%, and 0%, respectively. Inter-observer reliability between POCUS and conventional USG showed good agreement, with Cohen's kappa coefficients exceeding 0.8 for sensitivity and 0.6 for grading.ConclusionsRenal POCUS performed well in diagnosing and grading hydronephrosis in infants when performed by pediatric residents who had completed a two-phase training program

Delta neutrophil index as a predictor of vesicoureteral reflux in children with febrile urinary tract infection

Purpose Delta neutrophil index (DNI) indicates immature granulocytes in peripheral blood and has been confirmed to be effective as a prognostic factor for neonatal sepsis. Also, it has been reported to have diagnostic value in acute pyelonephritis and in predicting vesicoureteral reflux (VUR) in the infant. We conducted the study to verify whether DNI is also helpful in the entire pediatric age group with febrile urinary tract infection (UTI). Methods Medical records of children hospitalized for febrile UTIs were analyzed retrospectively. All subjects underwent kidney ultrasound and voiding cystourethrography. In the group with and without VUR, we compared sex and age, and the following laboratory values: the white blood cell count, neutrophil, polymorphonuclear leucocyte, eosinophil, hemoglobin, platelet count, C-reactive protein, DNI value, and the finding of ultrasound. Results A total of 315 patients (163 males and 152 females; range, 0–127 months) were eligible, and 41 patients (13%) had VUR. As a result of univariate analysis, the white blood cell count, neutrophil, DNI, and ultrasonic abnormalities were high in the reflux group, and the hemoglobin and lymphocyte fraction values were low. The value of DNI and the abnormal ultrasound were significantly higher in the reflux group on the multivariate analysis. The area under the curve value of the receiver operating curve was higher in DNI (0.640; 95% confidence interval, 0.536–0.744; P=0.004), and the DNI cutoff value for VUR prediction was 1.85%. Conclusions We identified that ultrasound findings and DNI values were helpful predictors of VUR in pediatric febrile UTIs

Anti-Forensic Trace Detection in Digital Forensic Triage Investigations

Anti-forensics, whether intentionally to disrupt investigations or simply an effort to make a computer system run better, is becoming of increasing concern to digital investigators. This work attempts to assess the problem of anti-forensics techniques commonly deployed in South Korea. Based on identified challenges, a method of signature-based anti-forensic trace detection is proposed for triage purposes that will assist investigators in quickly making decisions about the suspect digital devices before conducting a full investigation. Finally, a prototype anti-forensic trace detection system is given to demonstrate the practicality of the proposed method

Regulation of Microglia and Macrophage Polarization via Apoptosis Signal-Regulating Kinase 1 Silencing after Ischemic/Hypoxic Injury

Inflammation is implicated in ischemic stroke and is involved in abnormal homeostasis. Activation of the immune system leads to breakdown of the blood–brain barrier and, thereby, infiltration of immune cells into the brain. Upon cerebral ischemia, infiltrated macrophages and microglia (resident CNS immune cell) are activated, change their phenotype to M1 or M2 based on the microenvironment, migrate toward damaged tissue, and are involved in repair or damage. Those of M1 phenotype release pro-inflammatory mediators, which are associated with tissue damage, while those of M2 phenotype release anti-inflammatory mediators, which are related to tissue recovery. Moreover, late inflammation continually stimulates immune cell infiltration and leads to brain infarction. Therefore, regulation of M1/M2 phenotypes under persistent inflammatory conditions after cerebral ischemia is important for brain repair. Herein, we focus on apoptosis signal-regulating kinase 1 (ASK1), which is involved in apoptotic cell death, brain infarction, and production of inflammatory mediators after cerebral ischemia. We hypothesized that ASK1 is involved in the polarization of M1/M2 phenotype and the function of microglia and macrophage during the late stage of ischemia/hypoxia. We investigated the effects of ASK1 in mice subjected to middle cerebral artery occlusion and on BV2 microglia and RAW264.7 macrophage cell lines subjected to oxygen-glucose deprivation. Our results showed that ASK1 silencing effectively reduced Iba-1 or CD11b-positive cells in ischemic areas, suppressed pro-inflammatory cytokines, and increased anti-inflammatory mediator levels at 7 days after cerebral ischemia. In cultured microglia and macrophages, ASK1 inhibition, induced by NQDI-1 drug, decreased the expression and release of M1-associated factors and increased those of M2-associated factors after hypoxia/reperfusion (H/R). At the gene level, ASK1 inhibition suppressed M1-associated genes and augmented M2-associated genes. In gap closure assay, ASK1 inhibition reduced the migration rate of microglia and macrophages after H/R. Taken together, our results provide new information that suggests ASK1 controls the polarization of M1/M2 and the function of microglia and macrophage under sustained-inflammatory conditions. Regulation of persistent inflammation via M1/M2 polarization by ASK1 is a novel strategy for repair after ischemic stroke

Unusual Thymic Hyperplasia Mimicking Lipomatous Tumor in an Eight-Year-Old Boy with Concomitant Pericardial Lipomatosis and Right Facial Hemihypertrophy

We report a case of thymic hyperplasia accompanied by pericardial lipomatosis and right facial hemihypertrophy in an 8-year-old boy. On imaging studies, the hyperplastic thymus had prominent curvilinear and nodular fatty areas simulating a fat-containing anterior mediastinal mass, which is an unusual finding in children. To our knowledge, this is the first report on a child with a combination of thymic hyperplasia, pericardial lipomatosis, and right facial hemihypertrophy. The radiologic findings are presented with a brief discussion

BROADCAST ENCRYPTION π\pi

We propose a new broadcast encryption scheme $\pi$ based on the idea of `one key per each punctured interval\u27. Let $N$ and $r$ be the numbers of total users and revoked users, respectively. In our scheme with $p$-punctured $c$-intervals, the transmission overhead is asymptotically {\normalsize$\frac r{p+1}$} as $r$ grows. We also introduce two variants of our scheme to improve the efficiency for small $r$. Our scheme is very flexible with two parameters $p$ and $c$. We may take $p$ as large as possible if a user device allows a large key storage, and set $c$ as small as possible if the storage size and the computing power is limited. Our scheme also possesses another remarkable feature that any number of new users can join at any time without key refreshment, which is not possible in other known practical schemes

Transduction of the MPG-tagged fusion protein into mammalian cells and oocytes depends on amiloride-sensitive endocytic pathway

BACKGROUND: MPG is a cell-permeable peptide with proven efficiency to deliver macromolecular cargoes into cells. In this work, we examined the efficacy of MPG as an N-terminal tag in a fusion protein to deliver a protein cargo and its mechanism of transduction. RESULTS: We examined transduction of MPG-EGFP fusion protein by live imaging, flow cytometry, along with combination of cell biological and pharmacological methods. We show that MPG-EGFP fusion proteins efficiently enter various mammalian cells within a few minutes and are co-localized with FM4-64, a general marker of endosomes. The transduction of MPG-EGFP occurs rapidly and is inhibited at a low temperature. The entry of MPG-EGFP is inhibited by amiloride, but cytochalasin D and methyl-β-cyclodextrin did not inhibit the entry, suggesting that macropinocytosis is not involved in the transduction. Overexpression of a mutant form of dynamin partially reduced the transduction of MPG-EGFP. The partial blockade of MPG-EGFP transduction by a dynamin mutant is abolished by the treatment of amiloride. MPG-EGFP transduction is also observed in the mammalian oocytes. CONCLUSION: The results show that the transduction of MPG fusion protein utilizes endocytic pathway(s) which is amiloride-sensitive and partially dynamin-dependent. Collectively, the MPG fusion protein could be further developed as a novel tool of "protein therapeutics", with potentials to be used in various cell systems including mammalian oocytes

Trib2 regulates the pluripotency of embryonic stem cells and enhances reprogramming efficiency

Embryonic stem (ES) cells are pluripotent cells characterized by self-renewability and differentiation potential. Induced pluripotent stem (iPS) cells are ES cell-equivalent cells derived from somatic cells by the introduction of core reprogramming factors. ES and iPS cells are important sources for understanding basic biology and for generating therapeutic cells for clinical applications. Tribbles homolog 2 (Trib2) functions as a scaffold in signaling pathways. However, the relevance of Trib2 to the pluripotency of ES and iPS cells is unknown. In the present study, we elucidated the importance of Trib2 in maintaining pluripotency in mouse ES cells and in generating iPS cells from somatic cells through the reprogramming process. Trib2 expression decreased as ES cells differentiated, and Trib2 knockdown in ES cells changed their colony morphology while reducing the activity of alkaline phosphatase and the expression of the pluripotency marker genes Oct4, Sox2, Nanog and Klf4. Trib2 directly interacted with Oct4 and elevated Oct4 promoter activity. During the generation of iPS cells, Trib2 knockdown decreased the reprogramming efficiency of mouse embryonic fibroblasts, whereas Trib2 overexpression significantly increased their reprogramming efficiency. In summary, our results suggest that Trib2 is important for maintaining self-renewal in ES cells and for pluripotency induction during the reprogramming process